Gene calibration in the CRISPR Babies could upsurge the earlier death risk

The Chinese scientist He Jiankui, who revealed last fall that he used CRISPR gene editing to try to make twin newborn girls immune to HIV infection, might have also given them a higher risk of death. That’s according to a new study from University of California, Berkeley data scientists who analyzed the records of more than 400,000 people in the United Kingdom.

Looking at that large population sample, the Berkeley researchers studied the overall effects of the mutated gene that He Jiankui inserted into the embryos of the two girls with a single goal in mind—to protect them from the virus that causes AIDS.

The Berkeley study suggested that the gene mutation also comes with some significant downsides. The researchers compared death records and genomic profiles in the UK Biobank database.

They found that the death rate of people with one copy of Δ32 was the same as in people with no copies, which could have implications in the life spans of the two CRISPR babies. He Jiankui has said that one of the twins in his experiment was given two copies of CCR5-Δ32 —a homozygous mutation—and the other twin, just one copy of the mutated gene. The twin newborns are the first babies known to be the products of such an experiment.

He announced last fall that he and his colleagues had edited twin embryos, then reimplanted them in their mother’s womb. He refers to the girls as Lulu and Nana. He did the experiment at the Southern University of Science and Technology in Shenzhen, China. Officials there condemned his activities once they came to light.

Soon after that, scientists around the work began to dissect what kind of changes He might have made. Sean Ryder of the University of Massachusetts Medical School concluded that the changes He claims to have made does not match any of the “wild-type” Δ32 mutations found naturally in humans, most often in Northern Europeans. In other words, he had created edits with no known precedent. Ryder called it “unconscionable.”

CCR5 plays a wide role in humans, and tinkering with it gets complicated fast, Wei and Nielsen write: “A mutation can be advantageous or disadvantageous depending on environmental conditions and developmental stages.